ADAR Antibody | CSB-PA001324LA01HU

ADAR Antibody | CSB-PA001324LA01HU | Cusabio

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Product Type: Polyclonal Antibody

Target Names: ADAR

Aliases: Double-stranded RNA-specific adenosine deaminase (DRADA) (EC 3.5.4.37) (136 kDa double-stranded RNA-binding protein) (p136) (Interferon-inducible protein 4) (IFI-4) (K88DSRBP), ADAR, ADAR1 DSRAD G1P1 IFI4

Background: Catalyzes the hydrolytic deamination of adenosine to inosine in double-stranded RNA (dsRNA) referred to as A-to-I RNA editing. This may affect gene expression and function in a number of ways that include mRNA translation by changing codons and hence the amino acid sequence of proteins; pre-mRNA splicing by altering splice site recognition sequences; RNA stability by changing sequences involved in nuclease recognition; genetic stability in the case of RNA virus genomes by changing sequences during viral RNA replication; and RNA structure-dependent activities such as microRNA production or targeting or protein-RNA interactions. Can edit both viral and cellular RNAs and can edit RNAs at multiple sites (hyper-editing) or at specific sites (site-specific editing) . Its cellular RNA substrates include: bladder cancer-associated protein (BLCAP), neurotransmitter receptors for glutamate (GRIA2) and serotonin (HTR2C) and GABA receptor (GABRA3) . Site-specific RNA editing of transcripts encoding these proteins results in amino acid substitutions which consequently alters their functional activities. Exhibits low-level editing at the GRIA2 Q/R site, but edits efficiently at the R/G site and HOTSPOT1. Its viral RNA substrates include: hepatitis C virus (HCV), vesicular stomatitis virus (VSV), measles virus (MV), hepatitis delta virus (HDV), and human immunodeficiency virus type 1 (HIV-1) . Exhibits either a proviral (HDV, MV, VSV and HIV-1) or an antiviral effect (HCV) and this can be editing-dependent (HDV and HCV), editing-independent (VSV and MV) or both (HIV-1) . Impairs HCV replication via RNA editing at multiple sites. Enhances the replication of MV, VSV and HIV-1 through an editing-independent mechanism via suppression of EIF2AK2/PKR activation and function. Stimulates both the release and infectivity of HIV-1 viral particles by an editing-dependent mechanism where it associates with viral RNAs and edits adenosines in the 5'UTR and the Rev and Tat coding sequence. Can enhance viral replication of HDV via A-to-I editing at a site designated as amber/W, thereby changing an UAG amber stop codon to an UIG tryptophan (W) codon that permits synthesis of the large delta antigen (L-HDAg) which has a key role in the assembly of viral particles. However, high levels of ADAR1 inhibit HDV replication.

Isotype: IgG

Conjugate: Non-conjugated

Clonality: Polyclonal

Uniport ID: P55265

Host Species: Rabbit

Species Reactivity: Human

Immunogen: Recombinant Human Double-stranded RNA-specific adenosine deaminase protein (367-471AA)

Immunogen Species: Human

Applications: ELISA, WB, IHC

Tested Applications: ELISA, WB, IHC; Recommended dilution: WB:1:1000-1:5000, IHC:1:20-1:200

Purification Method: >95%, Protein G purified

Dilution Ratio1: ELISA:1:2000-1:10000

Dilution Ratio2: WB:1:1000-1:5000

Dilution Ratio3: IHC:1:20-1:200

Dilution Ratio4:

Dilution Ratio5:

Dilution Ratio6:

Buffer: Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4

Form: Liquid

Storage: Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.

Initial Research Areas: Microbiology

Research Areas: Epigenetics & Nuclear Signaling;Microbiology